F Jin, X Tao, H Wu, L Wu

Abstract

Tracheobronchomalacia (TBM) is a relatively rare but severe respiratory disease in children, characterised by softening and morphological changes of the trachea and bronchi, leading to respiratory distress. The aetiology of this disease remains poorly understood, and the absence of distinctive clinical features often leads to misdiagnosis. Bronchoscopy plays a pivotal role in the diagnosis and management of TBM. Although most cases of TBM are self-limiting, some children require clinical intervention. This article aimed to provide a comprehensive review of the latest advances in the diagnosis and management of TBM.

Introduction

Tracheomalacia (TM) refers to the excessive collapse of the trachea resulting from over-relaxation of the posterior wall (membranous part) or damage to the cartilaginous structure. When the main bronchi are also affected, the condition is termed tracheobronchomalacia (TBM). Conversely, if only the main bronchi are involved without tracheal lesions, the condition is referred to as bronchomalacia, which is relatively rare. According to the definition provided by the European Respiratory Society (ERS), TBM is characterised by a reduction of more than 50% in the airway lumen diameter during expiration under quiet breathing conditions.¹ This article provides a comprehensive overview of TBM's aetiology, pathophysiology, clinical manifestations, diagnosis, and treatment methods.

The concept of TM was introduced by Baxter and Dunbar in 1963,² describing a condition in which over-relaxation of the tracheal posterior wall (membranous part) or compromised cartilage integrity results in excessive tracheal collapse. The primary mechanism involves a dynamic increase in intrathoracic pressure due to expiratory recoil pressure of the chest wall, which is transmitted to the airways. In normal airways, changes in lumen diameter are negligible. However, in a softened airway, particularly when airflow obstruction leads to increased expiratory force, the tracheal or bronchial wall may collapse, causing partial or complete lumen occlusion.

Historically, relevant reports were scarce due to a limited understanding of TBM and constraints in diagnostic technology. With the increasing use of bronchoscopy, research on TBM has progressively advanced. Literature indicates that the incidence of TBM in the general population is approximately 4.5%, while among individuals undergoing bronchoscopy for chronic cough or bronchitis, the prevalence ranges from approximately 14.1% to 23.4%.³

Histopathology

The trachea comprises cartilage, smooth muscle fibres, and connective tissue. The cartilage forms a C-shape, accounting for approximately two-thirds of the tracheal circumference. The posterior one-third gap of the cartilage ring is closed by the membranous posterior wall, composed of smooth muscle and fibrous tissue. In 1980, Wailoo and Emery⁴ conducted autopsies on children. They found that in those without known congenital diseases but with a clear history of respiratory symptoms, the length of the tracheal membranous part was greater than the average normal value, and the cartilage-to-membranous part ratio was reduced. This reduction may suggest that the airway is more susceptible to collapse. They also observed that in children with tracheoesophageal fistula, cartilage deficiency accompanied by an increased length of the tracheal membranous part could similarly predispose to airway collapse.

Epidemiology

The literature suggests that congenital TBM is more prevalent in preterm infants, relatively more so in males under 2 years of age, and that bronchomalacia is comparatively more frequent.⁵ Ruben Boogaard et al conducted fiberoptic bronchoscopy on 512 children with chronic respiratory symptoms and found that 136 cases were diagnosed with congenital TM, accounting for 26.5%. Based on this, the estimated population incidence exceeds 1 in 2100.⁶ However, owing to the lack of specific manifestations of TBM, it is often underdiagnosed. Additionally, symptoms in some patients resolve with age, potentially leading to an underestimation of the actual incidence.⁷ With the continuous advancement and development of bronchoscopy technology, the detection rate of this disease is gradually increasing, but detailed reports on specific incidence and other epidemiological characteristics remain limited.

Classification and Aetiology

TBM generally encompasses TM, TBM, and bronchomalacia. The condition can be categorised into congenital and acquired types based on aetiology. Additionally, it can be classified as diffuse or localised according to the extent of the lesion. Furthermore, the severity of TBM varies and is typically categorised as mild, moderate, and severe.⁸

In many cases, the aetiology of TBM remains unclear. Congenital TBM is more common in preterm infants and occurs more frequently in males. This type of TBM may be related to abnormalities in cartilage development.⁹ Some studies indicate that congenital respiratory and gastrointestinal abnormalities, such as tracheoesophageal fistula and oesophageal atresia, may be associated with the condition.¹⁰ Additionally, several congenital syndromes, including CHARGE syndrome, trisomy 21 (Down syndrome), cri-du-chat syndrome, cardio-facial-cutaneous syndrome, DiGeorge syndrome, and mucopolysaccharidoses, have been reported in association with TBM.¹¹

Acquired TBM may be associated with various cardiovascular anomalies, such as double aortic arch, dilated cardiomyopathy, pulmonary artery sling, enlarged pulmonary arteries secondary to left-to-right shunt, right aortic arch, aberrant right subclavian artery, pulmonary vein enlargement, tetralogy of Fallot with absent pulmonary valve syndrome, left atrial hypertrophy, left atrial enlargement, severe pulmonary hypertension (PAH), and anomalous origin of the innominate artery. Skeletal abnormalities associated with TBM may include scoliosis and pectus excavatum. Infections and inflammatory processes, such as severe tracheobronchitis, persistent bacterial bronchitis, chronic suppurative lung diseases (including cystic fibrosis, primary ciliary dyskinesia, and other causes of bronchiectasis), relapsing polychondritis, and Stevens-Johnson syndrome, are also associated with TBM.

Tracheobronchial injuries caused by button batteries, delayed clearance of inhaled foreign bodies, and trauma may result in TBM. Treatments and surgical interventions related to TBM include prolonged intubation, tracheostomy, repair of tetralogy of Fallot, foetal balloon insertion for congenital diaphragmatic hernia, laryngotracheal reconstruction, tracheoplasty, and heart transplantation. Tumours and cysts associated with TBM may include primary tracheal tumours, teratomas, enterogenous cysts, cystic hygromas, thyroid masses, lymphatic malformations, thymomas, bronchogenic cysts, neuroblastomas, haemangiomas, and lymphomas.¹

No unified standard currently exists for assessing TBM severity. In 2019, the ERS formulated the TBM severity grading criteria as follows: mild TBM refers to a cross-sectional area reduction between 50% and 75%; moderate TBM involves a cross-sectional area reduction between 75% and 90%; and severe TBM corresponds to a cross-sectional area reduction exceeding 90%. With its clear quantitative indicators, recognition by international organisations, and ease of clinical application, this standard has gained widespread acceptance domestically and internationally.¹

Symptoms

Common signs and symptoms of TBM in children include a metallic or barking cough, recurrent and/or chronic respiratory infections, stridor, life-threatening episodic asphyxia, wheezing, respiratory noises, feeding difficulties, and dyspnoea. These signs and symptoms assist physicians in recognising and diagnosing TBM in children.^11,12 Symptoms in patients with primary non-syndromic TBM may spontaneously alleviate with age. This improvement is primarily attributed to increases in tracheal diameter, enhanced rigidity of the supporting cartilage, a more pronounced "C"-shaped cartilage rings, and reduced protrusion of the tracheal membranous portion as children grow.¹¹

Auxiliary Examinations

Pulmonary Function Tests (PFTs):
Several studies have explored the value of PFTs in diagnosing TBM, although these generally have small sample sizes, with only two reports,^6,13 including more than 20 participants. Pulmonary function test results are usually positively correlated with TBM severity. Therefore, lung function assessment can aid in diagnosing TBM, but cannot serve as a standalone diagnostic tool.¹⁴

Imaging Studies:
Chest X-ray:¹⁵ Currently, there is insufficient evidence to support the use of chest radiography in diagnosing TBM.

Fluoroscopy:¹⁶ Fluoroscopy can be employed as an initial screening method for TBM; however, due to its low resolution and limited diagnostic utility, chest X-ray is generally not the preferred method for diagnosing TBM. Chest X-ray combined with barium swallow imaging is commonly used to exclude stenosis caused by external compression.

Chest Computed Tomography:^17,18 Computed Tomography (CT) evaluates airway stenosis, dilation, and morphological abnormalities. Dynamic chest CT scans during expiratory and inspiratory phases can assess the airway dynamics and facilitate TBM diagnosis. CT also aids in evaluating treatment efficacy, such as postoperative airway improvement, and can identify compression factors, including vascular abnormalities, which may cause or exacerbate TBM.

Dynamic Magnetic Resonance Imaging:¹⁹ Magnetic resonance imaging (MRI) effectively avoids radiation exposure in children and demonstrates the airway cartilage and surrounding tissue structure. However, it has limitations: longer scan times, the requirement for patient immobility necessitating deep sedation or anaesthesia, and relatively low spatial resolution, which restricts its diagnostic efficacy in small infants.

Tracheobronchography:²⁰ Tracheobronchography is a safe technique with high temporal and spatial resolution, making it valuable for assessing TBM. However, this technique is not yet widely implemented domestically.

Bronchoscopy:^1,21,22
Bronchoscopy allows direct visualisation of the extent and length of TBM. However, as the bronchoscope occupies the airway cross-sectional area, it may increase airway pressure, potentially masking airway collapse. Moreover, even experienced bronchoscopists must rely on subjective evaluation of luminal changes. Image distortion due to bronchoscopic lens curvature and orientation, the small volume of the paediatric bronchial tree, and rapid breathing rate pose additional diagnostic challenges. Following an extensive literature review, the ERS continues to endorse bronchoscopy as the gold standard for diagnosing TBM. This recommendation is based on the relatively high sensitivity and specificity of bronchoscopy compared to other diagnostic methods. Bronchoscopy, performed by experienced physicians under controlled anaesthesia and in the absence of airway distortion from endotracheal intubation or laryngeal mask, can provide valuable diagnostic information.

Medical Treatment

Various medical treatments for TBM have been reported in the literature. However, as most cases of congenital TBM are self-limiting, diagnostic criteria remain inconsistent, the number of cases available for study is limited, and pre- and post-treatment evaluations are not comprehensive. These factors limit the development of standardised treatment strategies for TBM. The primary treatment methods currently include:

β₂ Adrenergic Receptor Agonists
Wheezing is a common symptom in patients with TBM, and bronchodilators play a significant role in its management. Patients with asthma comorbid with TBM may use bronchodilators to relax the smooth muscle of the central airway. However, the therapeutic efficacy of bronchodilators is not consistently optimal. The primary reason is that these drugs may exacerbate airway obstruction following a reduction in airway smooth muscle tone.²³

Ipratropium Bromide
A study found that 32 of 52 children with TBM exhibited symptomatic improvement following treatment with ipratropium bromide.²⁴ However, the study did not elucidate whether the improvement was attributable to its effects on airway secretions and/or airway tone.

Muscarinic Agonists (e.g., Bethanechol and Methacholine)
Muscarinic agonists may reduce tracheal compliance by inducing tracheal contraction.²⁵ However, this approach is not part of routine clinical practice. These agents primarily act on muscarinic receptors (M receptors) on airway smooth muscle, particularly M3 receptors. Activation of these receptors results in airway smooth muscle contraction, which may exacerbate airway obstruction.

Mucolytics
The use of mucolytics in TBM treatment has garnered some attention. A study²⁶ investigated the efficacy of nebulised recombinant human DNase (a mucolytic agent) in children with airway malacia and respiratory infections. The results indicated that 2 weeks of treatment did not significantly promote recovery or reduce the need for antibiotics. This finding suggests that although mucolytics may theoretically help improve airway secretion clearance, their clinical efficacy may not be as anticipated, at least in the short term, demonstrating limited therapeutic effects for patients with TBM. Therefore, the role of mucolytics in TBM treatment necessitates further research and evaluation.

Antibiotics
Antibiotics are not employed to treat TBM directly; however, bacterial infections can exacerbate symptoms of TBM, and studies have demonstrated that antibiotic treatment for at least 2 weeks can resolve most symptoms, although some children may experience recurrent symptoms.²⁷

Management of Comorbidities

Gastroesophageal Reflux
A study found that 70% of children aged 3 to 28 months with airway malacia had gastroesophageal reflux (GOR), compared with a 39% incidence of GOR in the control group.²⁸ This finding demonstrates a strong association between airway malacia and gastroesophageal reflux in children. However, it should be emphasised that this association does not imply causation.

Eosinophilic Esophagitis
Children with eosinophilic esophagitis comorbid with TBM appear to have poorer prognoses than those presenting solely with gastrointestinal symptoms. Among children who underwent oesophageal atresia repair, 17% developed oesophageal eosinophilia, and many of these children also had TBM.²⁹ Compared with the control group without eosinophilia, these children had significantly higher incidences of reflux symptoms, airway hyperreactivity, hypoxia (resulting from TBM and oesophageal dysfunction), and swallowing difficulties.^29,30

Respiratory Health Issues
All appropriate respiratory health measures should be emphasised, including but not limited to immunisations, influenza vaccinations, provision of a dry and warm living environment, proper exercise, and avoidance of passive smoking. Respiratory physiotherapy is commonly used in TBM management to enhance mucociliary clearance. However, based on our literature review, no studies have specifically investigated the effectiveness of physiotherapy in patients with TBM.³¹ Therefore, although respiratory physiotherapy is widely used in clinical practice, its specific role and effect in TBM management require further investigation.

Surgical Treatment

Surgical intervention, including stent implantation, may be necessary for patients presenting with symptoms such as apnoea, cyanosis, feeding difficulties, failure to wean from mechanical ventilation, and recurrent pneumonia. Comprehensive diagnostic evaluations assist in determining the most appropriate surgical technique. Surgical and endoscopic treatment options include tracheostomy, aortopexy, tracheal resection, tracheopexy (anterior or posterior), endoluminal stenting, and external airway splinting.¹⁶ During these procedures, intraoperative bronchoscopy may be particularly helpful in guiding surgeons. Indications for surgical intervention typically include severe symptoms consistent with significant expiratory airway obstruction demonstrated by PFTs, severe airway stenosis on imaging and bronchoscopy, recurrent pneumonia, difficulty in weaning from mechanical ventilation, intermittent airway obstruction, and when other treatment methods are ineffective or the patient's condition poses long-term health risks. The advantages and disadvantages of surgical and medical treatments are summarised in Table 1.

Tracheostomy: Once the mainstay of surgical treatment for TBM, tracheostomy is now generally considered a last resort. This procedure involves creating an incision through the anterior neck skin and trachea to insert a tracheostomy tube, thereby maintaining an open airway and facilitating respiration. Tracheostomy provides an internal airway stent and allows for long-term mechanical ventilation if necessary. However, it often results in prolonged dependence on an artificial airway, resulting in numerous complications that limit the application of this method in TBM management, including difficulties in extubation, tracheal spasm and stenosis, tracheal injury, secondary tracheal malacia, and repeated respiratory infection.¹⁶

Airway plasty: Airway plasty comprises various surgical methods to correct TM, adapted according to clinical presentation. Anterior aortopexy is primarily indicated for short-segment TM secondary to congenital tracheal occlusion (TOF).³² If bronchial collapse persists following aortopexy, pulmonary artery suspension surgery may be considered. Tracheal traction suturing techniques, also known as anterior tracheopexy, can provide more effective TM correction.³³ Posterior tracheopexy surgery involves stabilising the trachea by suturing the posterior tracheal membrane to the anterior longitudinal ligament of the spine via a right posterior thoracotomy.³⁴

Tracheectomy: In a limited number of carefully selected patients with short-segment TM, tracheal resection may be considered when other surgical or endoscopic techniques fail to achieve satisfactory outcomes. Furthermore, in patients with severe collapse above the tracheostomy site post-tracheostomy, known as peristomal TM, limited tracheal resection with end-to-end anastomosis is indicated.³⁵

Extratracheal stent immobilisation: This method can provide adequate airway support for highly selected cases, as an alternative to endoluminal stenting for patients with severe and/or diffuse TM/TBM. However, external splinting and tracheal reinforcement may lead to complications such as erosion into surrounding structures, potential choking effects following somatic growth in children, infection, and long-term tissue tolerance issues. These factors must be closely monitored when considering this method.³⁶ Absorbable external stents may become a new focus in the management of TBM. In recent years, the preliminary clinical application of 3D-printed bionic polycaprolactone (PCL) external tracheal stents in adult and paediatric patients with TM has been successful. This technology effectively supports patients with TM in maintaining normal tracheal morphology.³⁷

Airway Stent Implantation: Montgomery first proposed airway stenting in 1965, initially applying it to a 4-month-old female infant.³⁸ This approach is considered an appealing treatment concept. Most medical institutions reserve it as a last resort for children who are unsuitable for other surgical options and not candidates for tracheostomy. However, some institutions regard airway stenting as a viable alternative to tracheostomy. The primary advantage of stent implantation is that it does not require a thoracotomy and causes minimal trauma to the patient. Nevertheless, common clinical disadvantages are associated with this technique. These include susceptibility to granulation tissue proliferation, tearing of the membranous portion of the trachea, stent migration, impaired function of the normal tracheal epithelium, and, in severe cases, tracheal wall perforation. Additionally, stents may require expansion as children grow to accommodate anatomical changes. Following stent implantation, patients often experience immediate clinical improvement.³⁹

Continuous Positive Airway Pressure

Patients with TBM can be managed using various forms of non-invasive pressure ventilation, including continuous positive airway pressure (CPAP), bi-level positive airway pressure (BiPAP), high-flow nasal cannula oxygen therapy, and appropriate ventilatory support.¹¹ However, pressure support ventilation is generally not a standalone treatment for severe TBM. Instead, it is typically employed as an initial measure or adjunct to other treatment methods to provide symptomatic relief and respiratory support.

Conclusions

TBM lacks specific clinical manifestations, making it prone to misdiagnosis in clinical settings. Numerous challenges remain in its diagnosis and treatment that require further investigation. TBM management strategies vary depending on clinical symptoms, aetiology, age, disease severity, and other patient-specific factors. Therefore, treatment should be individualised. In terms of conservative management, continued research into the pathophysiological mechanism of TBM may facilitate the development of targeted pharmacotherapies. Advances in materials science and manufacturing processes, particularly in biocompatibility, may lead to more effective and safer interventions for stent therapy. In surgical management, combining traditional techniques with materials science or tissue engineering innovations holds promise for improved treatment outcomes. Notably, the use of absorbable external stents may represent an emerging area of research with significant therapeutic potential.

Declaration of Interest

All authors have disclosed no conflicts of interest.

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